~Atherosclerosis (Coronary Artery Disease), Part 4 - Herbal Supplements

~Atherosclerosis (Coronary Artery Disease), Part 4 - Herbal Supplements
Herbal Supplements
  • Bromelain
  • Curcumin
  • Garlic
  • Ginger
  • Ginkgo biloba
  • Green Tea Extract
One fourth of prescription drugs in the United States have at least one active ingredient derived from plant material. The World Health Organization estimates that 80% of the world population uses herbal treatments as part of their primary healthcare. Herbal extracts are among the most-studied preparations in the world. Most of modern medicine is directly or indirectly derived from folk medicine and herbal treatments.

Bromelain

Bromelain (Ananas comusus) is derived from the stem of the pineapple plant. Bromelain is a protein-digesting (proteolytic) enzyme capable of reducing atherosclerotic plaque. Proteolytic enzymes work directly at sites of inflammation, digesting damaged cell tissue (recall that inflammation is one of the newer risk factors recognized as a promoter of cardiac disease). Bromelain has fibrinolytic activities (the ability to break down fibrin). Fibrin forms a matrix that walls off an inflamed area, resulting in vessel blockage, inadequate tissue drainage, and edema (Felton 1980; Lotz-Winter 1990; Metzig et al. 1999; Maurer 2001). Bromelain may improve cardiac health by opposing platelet aggregation, and relieve angina attacks possibly through fibrinolytic properties. Bromelain is nontoxic up to 10 grams per kilogram. The only side effect noted has been allergic reactions in sensitive individuals (Murray 1995; Maurer 2001). Because bromelain is an anticoagulant it should be used with the advice of a physician if used with prescription anticoagulants. Individuals with cardiovascular disease who take bromelain should periodically have blood tests to measure their fibrinogen level to determine if serum fibrinogen is in a safe range.

Curcumin

Ground turmeric is used worldwide as a seasoning (as curry) and is a source for curcumin (turmeric contains approximately 4% curcumin). Turmeric is a member of the Curcuma botanical group, which is part of the ginger family of herbs (Zingiberaceae).

Curcumin has been used for over 3000 years in traditional Ayurvedic medicine, but more recently has showed cardiovascular-related activities (anti-platelet aggregating and anti-inflammatory activity) and antioxidant properties (Chainani-Wu 2003). Curcumin may control platelet aggregation by directly inhibiting thromboxane (a promoter of aggregation) and increasing prostacyclin activity (an inhibitor of aggregation). Some of curcumin's functions may lessen the risk of forming blood clots (Srivastava et al. 1985; Toda et al. 1985). Animal studies showed impressive cholesterol-lowering benefits. Rats fed 0.1% curcumin, on a cholesterol-containing diet, had one-half of the levels of blood cholesterol than rats without curcumin (Rao et al. 1970; Srivastava et al. 1986; Srinivasan et al. 1991).

Curcumin reduced serum levels of cholesterol and lipid peroxides in humans receiving 500 mg of curcumin daily for seven days (a short span of time to enact a change in lipid parameters). A significant decrease in the level of serum lipid peroxides (33%), an increase in HDL (29%), and a decrease in total serum cholesterol (12%) suggest that curcumin may prevent arterial diseases (Soni et al. 1992). A review of human trials determined that curcumin is without toxicity (Chainani-Wu 2003). If you are using a supplement called Super Curcumin with Bioperine in conjunction with drug therapy, your physician should be made aware of the supplementation. Piperine enhances the body's natural absorptive functions so it is possible bioperine may increase the absorption rate of drugs. The physician will schedule the dosages so that the drug and bioperine are taken at different times during the day. Because curcumin increases the excretion of cholesterol-bile acids, individuals with biliary tract obstruction should not use curcumin. Pregnant or lactating women should not use curcumin. High doses of curcumin taken on an empty stomach might cause stomach ulcers.

Garlic

High cholesterol (hypercholesterolemia) has been recognized as a risk factor in atherosclerosis. Oxidized LDL is a key player in the initiation and progression of atherosclerosis. Short-term supplementation of garlic in humans increased resistance of LDL to oxidation, suggesting that the suppression of LDL oxidation may be one mechanism for garlic's anti-atherosclerotic action (Lau 2001; Dillon et al. 2003). Garlic may reduce other risk factors in the genesis and progression of arteriosclerosis: garlic decreases total and LDL; increases HDL; reduces serum triglyceride and fibrinogen concentrations; lowers arterial blood pressure; inhibits platelet aggregation and reduces plasma viscosity (Siegel et al. 1999).

Reduction in arteriosclerotic plaque (5–18%) in femoral and carotid arteries of subjects receiving high-dose garlic was reported after continuous, high-dose garlic intake. These results substantiated that not only a preventive, but possibly also a curative role in arteriosclerosis therapy (plaque regression) may be ascribed to garlic remedies (Koscielny et al. 1999). Studies with 280 subjects showed a 9–18% reduction and a 3% regression in plaque volume following use of standardized garlic powder (900 mg). LDL decreased 4%, HDL increased 8%, blood pressure dropped by 7%, resulting in a reduced risk for infarction and stroke of over 50% (Siegel et al. 1999).

Ginger (Zingiber officinale)

Ginger may be of benefit in the fight against atherosclerosis. Ginger inhibits abnormal platelet aggregation through two mechanisms. It acts as a potent inhibitor of thromboxane synthetase, which increases the production of thromboxane A2. Thromboxane A2 makes platelets sticky, promoting blood clotting. Formation of thromboxane A2 is blocked by aspirin (AHA 2002b), but ginger also inhibits thromboxane synthesis. Unlike aspirin, ginger also raises prostacyclin, which inhibits abnormal platelet aggregation (Backon 1986). The maximum inhibitory values of gingerol G3 and G4 (the active components of ginger) were two-fold greater than aspirin (Koo et al. 2001).

Aqueous extracts of ginger, onion, and garlic were found to inhibit aggregation in a dose-dependent manner in vitro. There was a good correlation between the amount of ginger extract needed to inhibit platelet aggregation and platelet thromboxane synthesis (Srivas 1984).

Ginger can increase contractile strength of the heart (a "cardiotonic" function). Ginger may increase ATP production in the heart and enhance calcium transport within heart cells. Energy derived from ATP is necessary to transport calcium ions through membranes within heart muscle cells. The cycling of calcium within the heart, sustained by ATP, is vital to the development of contractile force (UM 1997).

Ginkgo Biloba

Two groups of substances possess pharmacological activity in ginkgo biloba: flavonoids, effective as oxygen-free radical scavengers, and terpenes (or ginkgolides), highly specific for their action as PAF inhibitors.

Important clinical indications for ginkgo biloba extracts are atherosclerotic disease of the peripheral arteries (intermediate severity) and cerebral insufficiency. Symptoms of cerebral insufficiency have been effectively and significantly influenced using ginkgo biloba extracts (Z'Brun 1995). Ginkgo has been used in the treatment of less severe cases of arteriosclerosis and orthostatic dysfunction (Uehleke 1994). Symptoms of orthostatic dysfunction include tachycardia, unstable blood pressure, lightheadedness, visual disturbances, and presyncope (temporarily reduction in oxygen to the brain, usually secondary to diminished blood flow).

Ischemia denotes a decreased supply of oxygenated blood to a tissue. Patients with stage II claudicating atherosclerotic arterial occlusive disease (ischemia) received 320 mg daily of ginkgo extract for 4 weeks. Subsequent tests showed that ischemic areas decreased by 38%. The rapid anti-ischemic action of ginkgo may be of value in the management of peripheral arterial occlusive disease at the stage of intermittent claudication (Mouren et al. 1994). Caution is advised when consuming more than 120 mg a day of ginkgo as excessive bleeding could result.

Green Tea Extract

Green tea is made from Camellia sinesis. Green tea contains polyphenols with antioxidant properties. Green tea extracts are used in Asia to lower blood pressure and reduce elevated cholesterol (ACS 2003). The ability of green tea to reduce cholesterol in rats was comparable to the drug probucol (Lorelco®, Bifenabid®), an antioxidant and hypocholesterolemic agent. Although higher amounts of polyphenol were needed to reduce total cholesterol and LDL levels (compared to probucol), green tea polyphenols effectively inhibited LDL oxidation and elevated serum anti-oxidative activity to the same degree as the drug. Green tea polyphenols increase HDL, leading to dose-dependent improvement of the atherogenic index, an effect not seen with probucol (Yokozawa et al. 2002).

The ability of green tea flavonoids to modify LDL oxidation was demonstrated in laboratory ODS rats unable to synthesize ascorbic acid (vitamin C). Rats on restricted dietary vitamin C showed deceased plasma ascorbic acid and a-tocopherol levels and an accelerated oxidation of LDL in vitro. Dietary green tea extract maintained plasma ascorbic acid and delayed LDL oxidation, suggesting flavonoids may suppress LDL oxidation by preserving levels of a-tocopherol in LDL or plasma levels of vitamin C (Kasaoka et al. 2002).

Antioxidants and flavonoids (in green tea) inhibit abnormal platelet aggregation associated with arterial clots preceding acute myocardial infarction or stroke. The predominant polyphenol found in green tea EGCG (epigallocatechin-3-gallate) inhibited platelet aggregation by hindering proteolysis of thrombin (Deana et al. 2003).

Side effects associated with green tea consumption are rare (aside from the occasional allergic reactions that always occur in the population). Green tea contains caffeine that acts as a stimulant, particularly in those who are sympathetic dominant. Decaffeinated green tea is an alternative choice. Pregnant or breast-feeding women should not drink green tea in large amounts (ACS 2003).

Trace Mineral Supplements

The US Department of Agriculture first suggested the importance of adequate mineral supplementation for cardiovascular disease (Anderson 1986).

"Evidence linking marginal intakes of the trace elements chromium, zinc and selenium with abnormal lipid metabolism and ultimately cardiovascular diseases is accumulating from both animal and human studies. Chromium supplementation of normal adult men as well as diabetics has been reported to increase HDL and decrease triglycerides and total cholesterol. Subjects with the highest total cholesterol and triglycerides usually respond the most to supplemental chromium. Selenium may also affect cardiovascular diseases since selenium is postulated to be involved in platelet aggregation. These data demonstrate that the trace elements chromium and selenium have beneficial effects on risk factors associated with cardiovascular diseases suggesting that a decreased risk of cardiovascular disease may be achieved by adequate intake of trace elements."

Trace elements such as selenium, zinc, and copper are essential for the activity of the antioxidant enzymes glutathione peroxidase and superoxide dismutase. Epidemiological studies suggested an increased risk of cardiovascular disease when blood concentrations of lipophilic antioxidants such as vitamin A, E, and beta-carotene are low.

Subjects with normal or elevated cholesterol who were treated by LDL-apheresis (to remove LDL from blood) were not deficient in vitamin E, beta-carotene, and copper, but did have low plasma levels of selenium, zinc, and vitamin A. The lower selenium and vitamin A levels resulted from LDL-apheresis; however, hypercholesterolemia may have caused the low levels of zinc. Supplementation of patients treated by LDL-apheresis should include selenium, zinc, and vitamin A (Delattre et al. 1998). A decrease in selenium levels parallels the increase in severity of CHD, suggesting an association of heart disease with subclinical levels of selenium. These trace elements might be used to assess the severity of CHD and adequate mineral intake might contribute to vascular disease therapy (Yegin et al. 1997).

Supplements for Healthy Coronary Arteries
  • Aspirin
  • Policosanol
  • TMG
  • Choline and Choline Derivatives
  • Creatine
Aspirin

Aspirin is used as a popular analgesic, but is also useful in maintaining cardiovascular health. Low-dose aspirin (81 mg) provides protection against abnormal blood clot formation via long-lasting effects on blood platelets. Platelets become less sticky so the risk of a heart attack and transient ischemic attacks is reduced (Diener 1998; Hart et al. 2000; Sacco et al. 2000; Califf et al. 2002).

Aspirin reduces C-reactive protein (CRP) and cardiac inflammation, which are newer risk factors in cardiovascular disease. Low-dose aspirin reduced heart attack risk by about 44% and the risk was 55% lower in men with high CRP levels. This suggests that aspirin's antagonism of platelet aggregation and its anti-inflammatory mechanisms combine to attenuate thrombosis (Physicians Weekly 1998).

Aspirin reduces inflammation by inhibiting the rate-limiting enzyme, cyclooxygenase that begins the inflammatory process (Newmark 2000). One molecule of aspirin will disable cyclooxygenase for 4–6 hours by acetylating the enzyme. (See C- Reactive Protein and the Link between Infections and Inflammation in Heart Disease in the protocol Cardiovascular Disease: Comprehensive Analysis to learn how inflammatory processes contribute to cardiac disease.)

An overview of four large-scale studies substantiated that aspirin therapy reduced nonfatal myocardial infarctions (MIs or heart attacks) by 32%. The researchers concluded that aspirin therapy could prevent a third of the MIs occurring in healthy individuals. There was a small but insignificant increase in the risk of vascular disease-related death and nonfatal stroke with aspirin therapy. When strokes were subdivided by type, there was no significant effect of aspirin therapy on the risk of ischemic stroke, but, while based on small numbers, there was a statistically significant 1.7-fold increase in the risk of hemorrhagic stroke (Hebert et al. 2000).

A large study over three years determined that aspirin was beneficial for individuals with coronary disease and reduced mortality risk (Gum et al. 2001).

Aspirin's benefit is greater among diabetic patients, significantly reducing the death rate from cardiac disease in diabetic patients with CHD. Diabetic patients using aspirin had a 11% mortality risk from cardiac diseases, while diabetic patients not using aspirin had a 16% risk (Harpaz et al. 1998).

Aspirin benefits carotid endarterectomy patients. Low-dose aspirin (81–325 mg daily) reduced risk of MI, stroke, and death following surgery. Individuals receiving 650–1300 mg were not similarly protected (Taylor et al. 1999).

All individuals over 50 years of age, with one cardiac risk factor and no condition that would negate treatment (e.g., increased prothrombin time, disturbed gastric mucosa, or hypertension), should consider using aspirin therapy. Note: Studies demonstrate that aspirin is not sufficient to prevent MI if fibrinogen levels are excessively high. Concomitant use of ibuprofen (but not rofecoxib, acetaminophen, or diclofenac) antagonizes the platelet inhibition caused by aspirin. Treatment with ibuprofen may limit the cardiovascular benefits of aspirin (Catella-Lawson et al. 2001).

A review of 287 studies involving 135,000 patients determined that over 40,000 lives are lost worldwide yearly because aspirin is underused. Aspirin (or other anti-platelet drugs) protects most patients at risk for occlusive vascular events (acute MI, ischemic stroke, unstable or stable angina, previous MI, cerebral ischemia, peripheral arterial disease, or atrial fibrillation) (ATC 2002). A daily dosage of 75–150 mg of aspirin is an effective anti-platelet regimen. An initial loading dose of at least 150 mg might be required in acute cases. Some clinical conditions are benefited by adding a second anti-platelet drug (ATC 2002). Aspirin can reduce the amount of damage to the heart during MI. Aspirin usage following a suspected heart attack is best chewed rather than swallowed, and is most beneficial if taken within 30 minutes of the onset of symptoms. Note: The use of warfarin alone or in combination with aspirin was superior to aspirin in reducing the severity of an acute MI. Warfarin is associated with a higher risk of bleeding (Hurlen et al. 2002).

CAUTION: Any amount of aspirin is contraindicated for individuals who are at risk for hemorrhagic stroke. If you take anticoagulants, have a blood clotting disorder, have experienced a hemorrhagic stroke, have experienced an allergic reaction to aspirin, or have a history of gastrointestinal ulcers, do not take any aspirin product without consulting your physician. Take aspirin with a meal to decrease stomach irritation. Discontinue taking aspirin two weeks before surgery. (Aspirin in low doses minimizes stomach irritation.)

Policosanol

Clinical trials using policosanol, derived from sugar cane, demonstrated similar clinical improvement in measures of cholesterol compared to commonly prescribed statin drugs such as Mevacor® (lovastatin), Zocor® (simvastatin), and Pravachol® (pravastatin) (Castano et al. 1999; Prat et al. 1999). Policosanol reduced harmful damaging LDL and increased the beneficial HDL. Policosanol (5 to 20 mg/day) decreased the risk of atheroma formation by reducing total cholesterol levels, inhibiting platelet aggregation, endothelial damage, and foam cell formation in animals (Varady et al. 2003).

Policosanol (20 mg/day) is as effective as 100 mg of aspirin per day in opposing platelet aggregation. Aspirin combined with policosanol is advantageous as each drug influences platelet activity through different mechanisms. (The combination of aspirin with other platelet inhibitors cannot be recommended without physician supervision.) Policosanol decreased systolic blood pressure providing an additional advantage for high-risk coronary patients (Arruzazabala et al. 1997; Castano et al. 2002).

Postmenopausal women receiving policosanol (5 mg/day for 8 weeks and 10 mg/day during the next 8 weeks) revealed decreased LDL levels (17% and 27%, respectively), total cholesterol levels (13% and 20%), and lower ratios of LDL to HDL (17.2% and 26.5%), and total cholesterol to HDL (16% and 21%). HDL levels were 7% higher at the end of the study. Policosanol was effective and well-tolerated in hypercholesterolemic postmenopausal women, showing additional health benefits for this subgroup (Mirkin et al. 2001).

No side effects are typically noted with policosanol therapy. Policosanol is available at less than half the cost of prescription statin medications. Side effects of nausea, headaches, dizziness, sleep disturbances, liver problems, muscle weakness, and pain reduce enthusiasm for statins by some practitioners. Policosanol does not interfere with the biosynthesis of coenzyme Q10 that is associated with statin usage. If you are already taking a prescription cholesterol medication, do not begin policosanol without physician consent.

TMG

TMG is used to lower homocysteine levels. Impaired homocysteine remethylation, induced by ethanol in animals, is reversed by TMG. TMG may be effective in correcting methylation defects (Barak et al. 2003). TMG lowers homocysteine, but regular dosing must continue to sustain this effect (Hoffman 1997; Fanapour et al. 1999; James et al. 2002; Baker-Racine 2002). There are no reports of side effects with TMG other than brief tension headaches when taken in large quantities without food. TMG should be taken with vitamin B12, B6, creatine, folic acid, and various sources of choline for homocysteine management.

Choline and Choline Derivatives

Any dietary supplement that contains choline or a choline derivative will lessen the need for SAMe. This is because much of the choline in the body is made by methylation reactions that require SAMe and generate homocysteine. This homocysteine must then be detoxified. Because homocysteine is linked to cardiovascular disease, supplements that reduce homocysteine production are potentially beneficial (Devlin 2002).

The biosynthesis of choline as phosphatidylcholine (lecithin) creates homocysteine in the liver for the synthesis of lipoproteins, especially HDL (Devlin 2002; Noga 2003; Lobley 1996). Circulating HDL contains an enzyme that allows HDL to remove free cholesterol from arterial cell walls for metabolism by the liver as HDL-cholesterol (Lehninger et al. 1993; Devlin 2002). This is why HDL-cholesterol is called the "good cholesterol".

To lower your homocysteine, increase intake of ‘pre-methylated' choline-containing products. Good sources of choline-containing products include: CDP-choline, a-GPC, lecithin and choline.

Creatine

Humans excrete 1,400 mg of creatinine in urine per day that must be replaced by the synthesis of creatine from SAMe (Devlin 2002). Supplemental creatine of 2-4 grams daily would probably cut production of homocysteine in half. Creatine supplementation reduces the formation of homocysteine and lessens the need to remethylate homocysteine back into methionine. Supplemental dietary creatine for two weeks lowered plasma levels of homocysteine by 25% (Stead et al. 2001). Doses of SAMe (1600 mg daily) increased phosphocreatine levels in human brain (Silveri et al. 2003), indicating that SAMe is important in the biosynthesis of creatine.

Continued . . .


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